This research examines how transplanted retinal pigment epithelium (RPE) and photoreceptors contribute to the restoration of structure and function in animal models of retinal degeneration. In RCS rats RPE transplants, bFGF and sham surgery retard the photoreceptor degeneration. We test a hypothesis that could explain these effects by the same mechanism, the removal by macrophages of a toxic factor produced by the pile up of outer segments in this genetic disease. We test whether bFGF recruits macrophages in the retina and whether these macrophages are related in space and time to the photoreceptor saving. We compare the ultrastructure of the photoreceptors rescued by bFGF, determine their proximity to macrophages; and compare them to photoreceptors saved by RPE transplants. Transplanted photoreceptors survive within the receptorless retinas of rd mice and RCS rats for at least three months. We determine whether transplants of retinal microaggregates lead to better photoreceptor preservation and function than dissociated photoreceptors when controlled for identical neonatal age. The ultrastructural morphology will be examined by electron microscopy, facilitated by a transgenic donor mouse with a reporter gene fused to a rhodopsin promotor; these transgenic rods uniquely express beta-galactosidase which allows their cytoplasm to be identified by electron microscopy. Photoreceptor function will be examined by the local ERG and trans-synaptic function by impulse recording and visually evoked cortical responses. A dye filled microelectrode will allow correlating responses with the transplant site in the retina.